The present invention relates generally to the field of development of muscle mass and body fitness; more specifically to a method utilizing a nicotine and/or nicotine acetylcholine receptor agonist supplement in combination with exercise to stimulate, recruit and mobilize new muscle cells to augment, strengthen or replace muscle cells in a mammalian body.
Development of muscle mass and body fitness is a multi-billion dollar industry worldwide. Myriad nutriceutical supplements and pharmacological medicines are utilized by wide ranging populations seeking to restore, augment or repair body tissues for both aesthetic and medical purposes. For example, stroke victims with muscle dystrophy require extensive rehabilitation of muscle use during recovery in order to restore muscle mass. Fitness devotees, and athletes seek to increase stamina, strength and muscle force in order to enhance personal appearance or performance. The very large population of persons wishing to aesthetically add muscle to body mass, replace fat with muscle or to simply increase strength in order to reduce fatigue stamina and/or appearance is accepted as a legitimate concern for good physiological and psychological health. Recent reports relate to anti-aging benefits when muscle-to-fat ratios are balanced.
Most, if not all health regimens relating to the above rely upon the effects of strenuous exercise programs supplemented with various nutritional diets. All require a relentless conformity to rigorous regimes, are costly and time consuming, and few result in any long-term success. Indeed, one of the common temptations for persons seeking to add muscle mass is the use of steroids, which have considerable negative side effects, including liver and heart damage.
It would seem that a process that enables the body to add or subtract various tissues through the use of the endogenous regulation of cells would be a major benefit to society. Recent reports of endogenous stem cells used to stimulate and promote the regrowth of de novo blood vessels to ischemic or injured tissues, such as the human heart, have been reported. Cooke J, et al., disclosed in PCT WO 01/08683 A1 the recruitment and mobilization of the body's own stem cells for building new blood vessels (angiogenesis) in blood-starved hind limbs in animals, through the use of nicotine in low dose forms. The cells that provided the new blood vessels originate, at least partly, in the patient's own bone marrow. Experiments demonstrated that after the animals were iatrogenically genically injured, then treated with nicotine, the area became mobilized with progenitor stem cells of both hematopoietic and mesenchymal lineage, which in turn differentiated into endothelial cells and smooth muscle cells. The use of nicotine for this purpose was also confirmed in a publication in the American Journal of Pathology, Vol. 161, No. 1, July 2002, Nicotine Accelerates Angiogenesis and Wound Healing in Genetically Diabetic Mice (Jacobi, et al). Scientists have reported that bone marrow stem cells injected directly into patients' hearts differentiated into cardiomyocyte (heart muscle) which repopulated the diseased and/or depleted muscle of the heart.